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G J Crystal

Publications and source records attributed to G J Crystal.

At least 37 records · Page 2Linked to original sources
PubMed1997

Role of adenosine triphosphate-sensitive potassium channels in coronary vasodilation by halothane, isoflurane, and enflurane.

BACKGROUND: Halothane, isoflurane, and enflurane cause coronary vasodilation and cardiac depression. This study was performed to assess the role of adenosine triphosphate (ATP)-sensitive potassium channels (KATP channels) in these effects. METHODS: Twenty-five thoracotomized dogs were anesthetized with fentanyl and midazolam. The left anterior descending coronary artery was perfused via either of two pressurized (80 mmHg) reservoirs. One reservoir was supplied with arterial blood free of a volatile anesthetic, and the second reservoir was supplied with arterial blood equilibrated in an oxygenator with a 1 minimum alveolar concentration of either halothane (0.9%, n = 10), isoflurane (1.4%, n = 8), or enflurane (2.2%, n = 7). Coronary blood flow (CBF) was measured using a Doppler flow transducer, and segmental shortening (SS) was measured with ultrasonic crystals. Responses to the volatile anesthetics were assessed under control conditions, during intracoronary infusion of the KATP channel inhibitor glibenclamide (100 micrograms/min), and after cessation of glibenclamide (recovery). The effectiveness of glibenclamide was verified from inhibition of coronary vasodilator responses to the KATP channel opener cromakalim without effect on those to the KATP channel-independent vasodilators, sodium nitroprusside and acetylcholine. RESULTS: Under control conditions, the volatile anesthetics caused pronounced increases in CBF (isoflurane > halothane = enflurane), and decreases in SS (enflurane > halothane = isoflurane). Glibenclamide blunted significantly (and reversibly) the increases in CBF, but it had no effect on the decreases in SS. CONCLUSIONS: The KATP channels play an important role in coronary vasodilation but apparently are not involved in cardiac depression caused by halothane, isoflurane, and enflurane in canine hearts in situ.

Adenosine Triphosphate↗
PubMed1996

Isoflurane-induced coronary vasodilation is preserved in reperfused myocardium.

Isoflurane causes vasodilation in the coronary circulation. The present study evaluated whether this action is preserved after a brief coronary occlusion followed by reperfusion. Fourteen open-chest dogs anesthetized with fentanyl and midazolam were studied. The left anterior descending coronary artery was perfused via an extracorporeal system with normal arterial blood or with arterial blood equilibrated with 1.4% (1 minimum alveolar anesthetic concentration [MAC]) isoflurane. Coronary perfusion pressure was maintained at 90 mm Hg. Coronary blood flow (CBF) was measured with a Doppler flow transducer. Steady-state changes in CBF during isoflurane, and during intracoronary infusions of acetylcholine (Ach; 20 micrograms/min), an endothelium-dependent vasodilator, and sodium nitroprusside (SNP; 80 micrograms/min), an endothelium-independent vasodilator, were compared in normal myocardium and in myocardium subjected to 15 min of ischemia (due to cessation of perfusion) followed by 30 min of reperfusion. Ischemia-reperfusion had no significant effect on the increases in CBF by isoflurane (421% +/- 88% vs 388% +/- 84%) or SNP (115% +/- 18% vs 135% +/- 19%), whereas it attenuated these increases in CBF by Ach (232% +/- 38% vs 143% +/- 21%). In conclusion, a brief period of myocardial ischemia followed by reperfusion did not affect the coronary vasodilating effects of isoflurane and SNP, although it blunted these effects of Ach. The present findings provide further evidence suggesting that the ability of isoflurane to relax coronary vascular smooth muscle is independent of the nitric oxide-cyclic guanosine monophosphate pathway.

Acetylcholine↗
PubMed1996

The direct effects of enflurane on coronary blood flow, myocardial oxygen consumption, and myocardial segmental shortening in in situ canine hearts.

This study evaluated changes in coronary blood flow (CBF), myocardial oxygen consumption (MVo2), and myocardial segmental shortening (SS) during intracoronary administrations of enflurane in in situ canine hearts. The left anterior descending coronary artery (LAD) of 11 anesthetized and mechanically ventilated dogs was perfused at constant perfusion pressure (80 mm Hg) with enflurane-free blood or with blood equilibrated in an extracorporeal oxygenator with enflurane (1.1%, 2.2%, 4.4%). CBF (measured with a Doppler flow transducer) was multiplied by the local arteriovenous (A-V) O2 difference to calculate MVo2. SS was measured with ultrasonic crystals. Myocardial lactate uptake was assessed. Peak CBF responses during enflurane were compared with those during maximum coronary vasodilation with adenosine. Enflurane caused concentration-dependent increases in CBF, and decreases in MVo2 and SS. The greatest increase in CBF during enflurane (4.4%) was similar to that achievable with adenosine. Myocardial lactate uptake was not affected by enflurane. In conclusion, enflurane has a direct coronary vasodilating effect. The potency of this effect is underscored by the ability of enflurane to cause marked increases in CBF, while appreciably reducing myocardial O2 demand. Since the enflurane-induced reduction in myocardial contractility was not due to ischemia, it likely reflected a direct negative inotropic effect. When the direct effects of enflurane are compared with those of equianesthetic concentrations of halothane and isoflurane previously shown in the same model, enflurane has a coronary vasodilating effect similar to that of halothane but less than that of isoflurane, and it has a negative inotropic effect greater than that of both isoflurane and halothane.

Anesthetics, Inhalation↗
PubMed1996

Investigations into the mechanisms of coronary vasodilation by contrast media in dogs.

RATIONALE AND OBJECTIVES: The study was performed to clarify the mechanisms underlying contrast-induced coronary vasodilation. METHODS: The left anterior descending coronary artery of 14 open-chest dogs was perfused at constant pressure. Coronary blood flow (CBF) was measured electromagnetically and used to calculate myocardial oxygen consumption (MVO2). Responses were evaluated during intracoronary infusions (2 mL/ minute) of the ionic contrast medium, Hypaque-76, and the nonionic contrast medium, Isovue-370, and compared with those caused by hypertonic saline solutions with comparable osmolarities. Studies also were conducted using Isovist-300, which is a new nonionic and iso-osmolar contrast medium. RESULTS: Hypaque-76 and Isovue-370 caused initial peak increases in CBF (reflecting decreases in coronary vascular resistance), which waned rapidly to achieve more modest steady-state increases within 2 to 3 minutes. Both the peak and steady-state increases in CBF were greater during Hypaque-76 than during Isovue-370. The increases in CBF caused by the contrast medium were greater than those caused by the corresponding saline solution. Neither Hypaque-76 nor Isovue-370 changed MVO2-Isovist-300 had no effect on CBF or MVO2. CONCLUSIONS: The coronary vasodilation by contrast media is the result of a direct vasorelaxing effect rather than secondary to a metabolic mechanism. Hyperosmolarity can account only in part for contrast-induced coronary vasodilation.

Animals↗
PubMed1996

Nitric oxide does not modulate myocardial contractility acutely in in situ canine hearts.

The study was designed to assess the influence of nitric oxide (NO) on myocardial contractility in vivo. The left anterior descending coronary artery (LAD) of 28 anesthetized, open-chest dogs was perfused with arterial blood via an extracorporeal circuit. In the LAD bed, segmental shortening (SS), an index of local myocardial contractility, was measured with ultrasonic crystals. Coronary blood flow (CBF) was measured by Doppler flow transducer and used to calculate myocardial oxygen consumption (MVO2). Studies were performed with coronary perfusion pressure (CPP) constant (n = 23) or with CBF constant (n = 5). Measurements were obtained 1) during intracoronary infusions of the NO donors sodium nitroprusside (SNP, 80 ng/min) and nitroglycerin (NTG, 40 micrograms/min) and of a stimulator of endogenous NO release, acetylcholine (ACh, 20 micrograms/min), and 2) after inhibition of basal NO synthase activity with either NG-nitro-L-arginine methyl ester (L-NAME, 300 micrograms/min ic for 15 min) or NG-monomethyl-L-arginine (L-NMMA 2mg/min ic for 15 min). Decreases in SS (-38%) and MVO2 (-42%) during intracoronary isoflurane infusion verified responsiveness of preparation to negative inotropic agents. With CPP constant, SNP, NTG, and ACh caused increases in CBF (177, 28, and 280%, respectively) with no changes in SS or MVO2. Neither L-NAME nor L-NMMA affected SS, MVO2, or CBF. With CBF constant, the SNP- and ACh-induced decreases in CPP were accompanied by no changes in SS. In conclusion, NO had no direct influence on myocardial contractility or oxygen demand under baseline conditions, or when its local concentration was increased acutely with SNP, NTG, or ACh. An augmented SS secondary to increased CBF per se, i.e., Gregg's phenomenon, did not obscure potential negative inotropic effects of SNP and ACh with CPP constant.

Acetylcholine↗
PubMed1995

Direct effects of halothane on coronary blood flow, myocardial oxygen consumption, and myocardial segmental shortening in in situ canine hearts.

Previous in vivo studies of the coronary vascular effects of halothane (HAL) were complicated by varying hemodynamic conditions and global cardiac work demands. Accordingly, the current study evaluated changes in coronary blood flow (CBF) and associated variables during selective intracoronary administrations of HAL in in situ canine hearts using an extracorporeal-controlled pressure perfusion system. Findings during HAL were compared to those during isoflurane (ISO). The left anterior descending coronary artery (LAD) of 8 open-chest dogs anesthetized with fentanyl and midazolam was perfused at constant pressure (109 +/- 2 mm Hg) with HAL-free arterial blood or with blood equilibrated in an extracorporeal oxygenator with HAL (0.5%, 1.0%, 2.0% in 95% O2-5.0% CO2). In the LAD bed, measurements of CBF were obtained with an electromagnetic flowmeter and used to calculate myocardial oxygen consumption (MVO2). Percent segmental shortening (%SS) was measured with ultrasonic crystals. Changes in CBF by HAL were compared to those during maximal vasodilation with adenosine. Separate studies (n = 5) were performed using 1.4% [1 minimum alveolar anesthetic concentration (MAC)] ISO and the findings compared to those during an equianesthetic (1.0%) concentration of HAL. HAL caused concentration-dependent increases in CBF, and decreases in MVO2 and %SS. With 2.0% HAL, the level of CBF was 50% of the maximal adenosine-induced response. At equianesthetic concentrations, HAL caused increases in CBF that were one-third of those caused by ISO, while the decreases in MVO2 and %SS caused by the drugs were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1995

Hemodilution impairs hypocapnia-induced vasoconstrictor responses in the brain and spinal cord in dogs.

Despite the increasing use of plasma expanders in the perioperative period, there have been few studies of cerebrovascular responsiveness during hemodilution. The present study was performed to evaluate the influence of isovolemic hemodilution on vasoconstrictor responses in the brain and spinal cord during hypocapnia. Sixteen mechanically ventilated, halothane-anesthetized dogs were randomly divided into two equal groups: Group 1, control group (hematocrit [Hct], 42% +/- 2%); Group 2, isovolemic hemodilution with 5% dextran 40 (Hct, 19% +/- 2%). Hypocapnia (22 +/- 1 mm Hg) was induced in both groups by removal of dead space tubing without altering mechanical ventilation. Regional blood flow in the brain and spinal cord was measured with 15-microns radioactive microspheres and used to calculate regional vascular resistance (RVR). In Group 1, hypocapnia caused increases in RVR (ranging from 44% +/- 10% in the cerebral cortex to 93% +/- 17% in the thoracic spinal cord). In Group 2, hemodilution itself decreased RVR relatively uniformly throughout the brain and spinal cord. After hemodilution, hypocapnia had no significant effect on RVR in the cerebral cortex, cerebellum, pons, and medulla, and caused less pronounced increases in RVR within the spinal cord. We conclude that hemodilution either attenuated or completely abolished vasoconstrictor responses within the brain and spinal cord during hypocapnia. Furthermore, the present findings suggest that induced hypocapnia may be less effective as a clinical maneuver to reduce increased intracranial pressure during hemodilution.

Animals↗
PubMed1995

Coronary vasodilation by isoflurane. Abrupt versus gradual administration.

BACKGROUND: Under certain circumstances, isoflurane is associated with coronary artery vasodilation. The objective of the current study was to ascertain whether the rate of administration of isoflurane influences its vasodilating effect in the coronary circulation. METHODS: Seven open-chest dogs anesthetized with fentanyl and midazolam were studied. The left anterior descending coronary artery was perfused via either of two pressurized (80 mmHg) reservoirs; reservoir 1 (control) was supplied with arterial blood free of isoflurane, and reservoir 2 was supplied with blood from an extracorporeal oxygenator, which was provided with 95% O2/5% CO2 gas that passed through calibrated vaporizer. Coronary blood flow (CBF) was measured with Doppler flow transducer. In each dog, isoflurane was administered according to two protocols; abrupt (isoflurane-A) or gradual (isoflurane-G). In isoflurane-A, the left anterior descending coronary artery was switched from reservoir 1 to reservoir 2 after the latter was filled with blood previously equilibrated with 1.4% (1 MAC) isoflurane. In isoflurane-G, the left anterior descending coronary artery was switched to reservoir 2 with vaporizer set at 0% isoflurane; then the vaporizer was adjusted to 1.4% isoflurane, which produced a gradual increase in isoflurane concentration within reservoir 2 that reached a level equivalent to that in isoflurane-A (as evaluated by gas chromatography) by 30 min. CBF during maximally dilating, intracoronary infusion of adenosine served as a reference to assess effects of isoflurane. RESULTS: Isoflurane-A caused marked increases in CBF, which, at constant perfusion pressure, reflected pronounced reductions in vascular resistance. These increases in CBF were 80% of those with adenosine. Although isoflurane-G also caused increases in CBF, the increases were only 45% of those caused by isoflurane-A. CONCLUSIONS: The current findings demonstrate that the extent of coronary vasodilation by isoflurane was not dependent only on its blood concentration but also on the rate at which this blood concentration was achieved; a gradual increase in blood concentration blunted the vasodilator effect. Differences in the rate of administration of isoflurane likely contributed to its widely variable coronary vasodilating effects in previous studies.

Adenosine↗
PubMed1995

Contribution of nitric oxide to coronary vasodilation during hypercapnic acidosis.

The present study was performed to evaluate the role of nitric oxide (NO) in coronary vasodilation during hypercapnic acidosis (HC). The left anterior descending coronary arteries of 17 anesthetized, open-chest dogs were perfused with normal arterial blood or with arterial blood equilibrated in an extracorporeal circuit with 90% O2-10% CO2 [arterial carbon dioxide tension (PaCO2) 72 +/- 3 mmHg, arterial pH 7.16 +/- 0.02]. Coronary perfusion pressure (CPP) was initially set at 100 mmHg. Coronary blood flow (CBF) was measured with a Doppler transducer. Studies were conducted under constant-pressure (variable CBF; n = 13) and constant-flow (variable CPP) conditions (n = 4). Steady-state changes in CBF (or CPP) during HC and during intracoronary infusions of acetylcholine (ACh, 20 micrograms/min), an endothelium-dependent vasodilator, and sodium nitroprusside (SNP, 80 micrograms/min), an endothelium-independent vasodilator, were compared before and after intracoronary infusion of a NO synthase inhibitor, either NG-nitro-L-arginine methyl ester (L-NAME, 4.5 mg) or NG-monomethyl-L-arginine (L-NMMA, 30 mg). Under constant pressure, L-NAME blunted increases in CBF by HC (274 +/- 32 vs. 113 +/- 24%) and ACh (400 +/- 43 vs. 68 +/- 17%), whereas increases in CBF by SNP were not significantly affected (207 +/- 34 vs. 186 +/- 18%). Results with L-NMMA were similar. Under constant flow, L-NAME attenuated decreases in CPP by HC and ACh, whereas it had no significant effect on decreases in CPP by SNP. In conclusion, HC elicits release of NO from coronary vascular endothelium via a direct effect rather than secondary to an increased flow rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1994

Myocardial oxygen supply-demand relations during isovolemic hemodilution.

The findings presented in this article pertain strictly to the specific conditions of the studies and should be extrapolated to human patients with caution for several reasons. First, the experimental model of a single acute coronary stenosis is a rare clinical occurrence, and it ignores the influence of the well-developed collateral circulation and impaired endothelial function which may accompany long-standing coronary artery disease (22). Second, the absolute hematocrit at which cardiac dysfunction arises would likely vary if a different anesthetic technique or diluent were used, or if the study were carried out in the absence of thoracotomy and positive-pressure ventilation or at a reduced body temperature. Nevertheless, the present findings provide broad guidelines for assessing when hemodilution may be used safely as a method of blood conservation. They suggest (1) that relatively severe hemodilution alone or moderate hemodilution combined with controlled hypotension with either SNP or ADEN may be used safely if cardiac function is normal and the coronary circulation is not obstructed, but (2) that even moderate hemodilution alone may be unsafe in patients in whom the coronary vasodilator reserve is exhausted or severely depleted by a proximal stenosis.

Animals↗
PubMed1994

Nitric oxide does not mediate coronary vasodilation by isoflurane.

BACKGROUND: Isoflurane causes vasodilation in the coronary circulation. The current study employed a canine model permitting selective intracoronary administrations of isoflurane (1) to test the hypothesis that coronary vasodilation by isoflurane is mediated by nitric oxide and (2) to evaluate the persistence of coronary vasodilation during an extended exposure to isoflurane. METHODS: Open-chest dogs anesthetized with fentanyl and midazolam were studied. The left anterior descending coronary artery (LAD) was perfused via extracorporeal system with normal arterial blood or with arterial blood equilibrated with 1.4% (1 MAC) isoflurane. In the LAD bed, coronary blood flow (CBF) was measured with an electromagnetic flowmeter and used to calculate myocardial oxygen consumption (MVO2). In series 1, performed at constant coronary perfusion pressure (CPP), the LAD was exposed to 3 h of isoflurane in two groups of eight dogs: control group, normal coronary endothelium; and experimental group, intracoronary infusion of the nitric oxide synthase inhibitor L-NAME (0.15 mg/min for 30 min). Series 2 was performed with CBF constant; thus, CPP varied directly with coronary vascular resistance. In this series, initial steady-state changes in CPP by isoflurane were evaluated in the same four dogs before and after L-NAME. RESULTS: In the control group of series 1, isoflurane caused a maximal, initial increase in CBF of 444%; however, CBF decreased progressively reaching a value not significantly different from baseline after 3 h of isoflurane. Isoflurane caused a significant (approximately 35%) decrease in MVO2, which persisted during the 3-h administration. Findings after L-NAME (experimental group) were not significantly different from those in control group. In series 2, isoflurane caused significant decreases in CPP that were not affected by L-NAME. CONCLUSIONS: The lack of effect of L-NAME on isoflurane-induced coronary vasodilation suggests that nitric oxide does not mediate this response. The increase in CBF during prolonged isoflurane waned over time, perhaps because of tachyphylaxis or emergence of a competitive vasoconstrictor mechanism, e.g., metabolic factors secondary to reduced oxygen demands.

Animals↗
PubMed1994

Effect of intracoronary infusions of amrinone and dobutamine on segment shortening, blood flow, and oxygen consumption in in situ canine hearts.

Previous in vivo studies assessing the effects of amrinone on myocardial contractility used intravenous infusions, and thus were complicated by varying cardiac loading conditions. Accordingly, the present study was performed in 15 open-chest, anesthetized (fentanyl and midazolam) dogs using infusions of amrinone and dobutamine directly into the left anterior descending artery (LAD). In the LAD bed, percentage of segment shortening (%SS), an index of local myocardial contractility, was assessed with ultrasonic crystals. Coronary blood flow was measured electromagnetically and used to calculate myocardial oxygen consumption and infused drug concentrations. Amrinone and dobutamine were infused separately into the LAD at rates yielding calculated arterial blood concentrations in the clinical range (100, 150, and 200 micrograms/min, and 2.5, 5.0, and 7.5 micrograms/min, respectively). A mixture of amrinone and dobutamine was also infused into LAD and changes in %SS compared with the sum of the their individual effects. In six of the dogs, an extracorporeal system was used to maintain constant coronary blood flow during amrinone infusions. Amrinone and dobutamine caused individually increases in %SS that were comparable (range, 20%-45%). Myocardial oxygen consumption increased in parallel with %SS for both amrinone and dobutamine. For amrinone, coronary blood flow increased more than myocardial oxygen consumption, resulting in a modest (at highest dose approximately 10%) decrease in oxygen extraction; whereas for dobutamine, coronary blood flow increased in proportion to myocardial oxygen consumption, resulting in no change in oxygen extraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Amrinone↗
PubMed1994

Effects of hypertonic saline solutions in the coronary circulation.

UNLABELLED: The use of small-volume injections of hypertonic saline solutions (HSS) in resuscitation from hemorrhagic shock is accompanied by well-maintained and pronounced increases in coronary blood flow (CBF) and by increases in myocardial contractility. The present study was performed in open-chest, anesthetized dogs to evaluate the contribution of direct coronary vasodilator and positive inotropic effects of HSS to these therapeutic responses. The left anterior descending coronary artery (LAD) was cannulated and perfused at constant pressure (100 mm Hg) with normal arterial blood. CBF in LAD was measured electromagnetically, and used to calculate myocardial oxygen consumption (MVO2) and coronary arterial plasma osmolality. Percent segmental shortening in LAD bed (% SS) was evaluated with ultrasonic crystals. Measurements were obtained during infusion into LAD of 2.5, 5.0, and 7.5% HSS at 2 ml/min. These HSS solutions yielded calculated plasma osmolalities of 329 +/- 3, 361 +/- 8, and 378 +/- 10 mOsm/kg, respectively. The increases in plasma osmolality by 2.5% HSS were in the therapeutic range, whereas those by 5.0 and 7.5% HSS were supertherapeutic. HSS caused initial peak increases in CBF (reflecting decreases in coronary vascular resistance), which waned rapidly to achieve modest steady-state increases within 2-3 min. The magnitude of the peak and steady-state increases in CBF by HSS correlated to osmolality. The 2.5% HSS had no effect on MVO2 and % SS, whereas the 5.0% and 7.5% HSS increased these variables in an osmolality-dependent manner. CONCLUSIONS: (1) intracoronary infusions of HSS caused modest steady-state coronary vasodilation, (2) Supertherapeutic elevations of plasma osmolality by HSS were required for direct positive inotropic effects, and (3) the present findings suggest that the direct cardiac actions of HSS contribute minimally to the increases in coronary blood flow and myocardial contractility that follow the use of these solutions for resuscitation from hemorrhagic shock.

Animals↗
PubMed1993

Limit to cardiac compensation during acute isovolemic hemodilution: influence of coronary stenosis.

We assessed limit to cardiac compensation during isovolemic hemodilution (HD) in 14 anesthetized dogs. Radioactive microspheres were used to evaluate myocardial blood flow (MBF) and its transmural distribution (endo/epi). Myocardial O2 consumption (MVO2) and percent lactate extraction were determined. Coronary vasodilator reserve was assessed from reactive hyperemic responses. Dogs were divided into group 1, with intact left anterior descending coronary artery (LAD), and group 2, with critical stenosis of LAD. Measurements were obtained at baseline and during graded HD (Hespan) until cardiac failure (CF). CF occurred at lower hematocrit in group 1 compared with group 2 (9 +/- 1 vs. 17 +/- 1%). In group 1, MBF increased during HD to maintain MVO2 constant; increases in MBF were transmurally uniform until CF, when decreased endo/epi and lactate production suggested subendocardial ischemia. Coronary vasodilator reserve decreased progressively during HD and was absent at CF. In group 2, stenotic LAD demonstrated constant MBF (resulting in decreased MVO2) during HD. At CF, these responses along with reduced endo/epi and lactate production indicated local myocardial ischemia. We conclude that 1) with normal coronary circulation, cardiac function was well maintained over a wide range of hematocrits because increases in MBF were transmurally uniform and sufficient to maintain myocardial oxygenation: CF occurred during extreme HD when MBF became maldistributed, resulting in subendocardial ischemia; 2) critical coronary stenosis impaired coronary vascular adjustment to HD and reduced significantly tolerance of left ventricle to HD; and 3) present findings underscore the importance of recruitment of coronary vasodilator reserve in preserving total and regional myocardial oxygenation during HD.

Adaptation, Physiological↗
PubMed1993

Right and left ventricular O2 uptake during hemodilution and beta-adrenergic stimulation.

Myocardial O2 uptake (MVO2) and related variables were compared in right and left ventricles (RV and LV, respectively) during isovolemic hemodilution (HD) alone and combined with isoproterenol (Iso) infusion in 13 isoflurane-anesthetized open-chest dogs. Measurements of myocardial blood flow (MBF) obtained with radioactive microspheres were used to calculate MVO2. Lactate extraction (Lacext) was determined. The study consisted of two experimental series: 1) graded HD (dextran) to hematocrit (Hct) of 10% and 2) Iso (0.1 microgram.kg-1.min-1 iv) during moderate HD (Hct = 18 +/- 1%). In series 1, arteriovenous O2 content difference in both ventricles decreased in parallel with reduced arterial O2 content caused by HD, i.e., percent O2 extraction was constant; MVO2 was maintained by proportional increases in MBF. In series 2, Iso during moderate HD raised MVO2 (RV, +156%; LV, +80%). Higher MVO2 was satisfied by combination of increased MBF and O2 extraction in RV and by increased MBF alone in LV. Lacext remained consistent with adequate myocardial O2 delivery throughout study. Conclusions were that 1) both RV and LV tolerated extreme HD (Hct = 10%) because blood flow reserves were sufficient to fully compensate for reduced arterial O2 content; 2) significant cardiac reserve was evident during HD, which could be recruited Iso; and 3) because increase in MVO2 in RV caused by Iso in presence of HD was partially satisfied by increased O2 extraction, the absence of augmented O2 extraction during HD alone was not due to impaired release of O2 from diluted red blood cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Direct effects of propofol on myocardial contractility in in situ canine hearts.

The pronounced decrease in arterial blood pressure evident during anesthetic induction with propofol has raised the possibility that propofol has a direct negative inotropic effect. Previous attempts to evaluate this mechanism in vivo have been inconclusive because of confounding variables associated with intravenous administration of propofol. Accordingly, in the current study, steady-state changes in myocardial contractility and related hemodynamic parameters were assessed during intracoronary infusions of propofol in seven open-chest dogs anesthetized with fentanyl and midazolam. The left anterior descending coronary artery (LAD) was cannulated and perfused at controlled pressure (100 mmHg) with normal arterial blood. In LAD-perfused myocardium, contractility was evaluated from measurements of percent segmental shortening (%SS) obtained with ultrasonic crystals. Coronary blood flow in LAD was measured electromagnetically and used to calculate myocardial oxygen consumption (MVO2; Fick principle) and coronary propofol concentration. Propofol was infused into the LAD at 150, 300, 600, and 1,200 micrograms/min (P-150, P-300, P-600, P-1,200). These infusion rates yielded calculated blood concentrations of 7 +/- 1, 15 +/- 1, 26 +/- 2, and 50 +/- 5 micrograms.ml-1, respectively. The calculated blood concentrations at P-150 were in the clinical range, whereas those at P-300, P-600, and P-1,200 were supratherapeutic. P-150 had no effect on %SS, whereas higher infusion rates caused decreases in %SS. Changes in MVO2 by propofol generally paralleled changes in %SS. At P-150 and P-300, coronary blood flow was proportional to MVO2, whereas at P-600 and P-1,200, coronary blood flow was in excess of the prevailing MVO2, resulting in increased coronary venous oxygen tension.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗